Chronic inhalation of coal dust can cause several lung disorders, including simple coalworkers pneumoconiosis (CWP), progressive massive fibrosis (PMF), chronic bronchitis, lungfunction loss, and emphysema. This review focuses on the cellular actions and interactions ofkey inflammatory cells and target cells in coal dust toxicity and related lung disorders, i.e.macrophages and neutrophils, epithelial cells, and fibroblasts. Factors released from or affectingthese cells are outlined in separate sections, i.e. (1) reactive oxygen species (ROS) and relatedantioxidant protection mechanisms, and (2) cytokines, growth factors and related proteins.Furthermore, (3) components of the extracellular matrix (ECM), including the modifying role ofROS, cytokines, proteases and antiproteases are discussed in relation to tissue damage andremodelling in the respiratory tract.It is recognised that inhaled coal dust particles are important non-cellular and cellularsources of ROS in the lung, and may be significantly involved in the damage of lung target cellsas well as important macromolecules including α-1-antitrypsin and DNA. In vitro and in vivo studies with coal dusts showed the up-regulation of importantleukocyte recruiting factors, e.g. Leukotriene-B4 (LTB4), Platelet Derived Growth Factor(PDGF), Monocyte Chemotactic Protein-1 (MCP-1), and Tumor Necrosis Factor-α(TNFα), as well as the neutrophil adhesion factor Intercellular Adhesion Molecule-1(ICAM-1). Coal dust particles are also known to stimulate the (macrophage) production ofvarious factors with potential capacity to modulate lung cells and/or extracellular matrix,including O2 · −, Hfn2fn2Nitric oxide is strictly not to beconsidered as ROS (i.e. oxygen-centered radical), but comprises a major source of reactive(oxygen) species, including ONOO−, OH·, and singlet oxygen.O2, and NO·, fibroblast chemoattractants (e.g. TransformingGrowth Factor-β (TGFβ), PDGF, and fibronectin) and a number of factors thathave been shown to stimulate and/or inhibit fibroblast growth or collagen production such as(TNFα, TGFβ, PDGF, Insulin Like Growth Factor, and Prostaglandin-E2). Further studies are needed to clarify the in vivo kinetics and relative impact ofthese factors.